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Books on the topic 'Reactive oxigen species (ROS)'

Author: Grafiati

Published: 9 March 2023

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1

Musonda, Alam Clement. Quercetin as a modulator of xenobiotic metabolism and reactive oxygen species (ROS) in human hepG2 cells. Birmingham: University of Birmingham, 1998.

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2

Nakamura, Tomohiro, and Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.

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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.

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3

Filip, Cristiana, and Elena Albu, eds. Reactive Oxygen Species (ROS) in Living Cells. InTech, 2018. http://dx.doi.org/10.5772/intechopen.69697.

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4

Zilliox, Lindsay, and James W. Russell. Diabetic and Prediabetic Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0115.

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Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxidative species can alter mitochondrial function, protein and DNA structure, interfere with signaling pathways, and deplete antioxidant defenses. Advanced glycelation end (AGE) products and formation of ROS are activated by and in turn regulate key signal transduction pathways.

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5

TG 495: Ros (Reactive Oxygen Species) Assay for Photoreactivity. OECD, 2019. http://dx.doi.org/10.1787/915e00ac-en.

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6

Singh, Vijay Pratap, Sheo Mohan Prasad, Durgesh K. Tripathi, Samiksha Singh, and Devendra K. Chauhan. Reactive Oxygen Species in Plants: Boon or Bane - Revisiting the Role of ROS. Wiley & Sons, Limited, John, 2017.

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7

Reactive Oxygen Species in Plants: Boon Or Bane - Revisiting the Role of ROS. Wiley, 2017.

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8

Singh, Vijay Pratap, Sheo Mohan Prasad, Durgesh Kumar Tripathi, Devendra Kumar Chauhan, and Samiksha Singh. Reactive Oxygen Species in Plants: Boon or Bane - Revisiting the Role of ROS. Wiley & Sons, Incorporated, John, 2017.

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9

Singh, Vijay Pratap, Sheo Mohan Prasad, Durgesh Kumar Tripathi, Devendra Kumar Chauhan, and Samiksha Singh. Reactive Oxygen Species in Plants: Boon or Bane - Revisiting the Role of ROS. Wiley & Sons, Incorporated, John, 2017.

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10

Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier, 2020. http://dx.doi.org/10.1016/c2019-0-04102-7.

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11

Madkour, Loutfy H. Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier Science & Technology Books, 2020.

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12

Oxidology the Study of Reactive Oxygen Species (Ros) and Their Metabolism in Health and Disease. 2nd ed. Bradford Foundation, 1997.

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13

Curtis, William, Martin Kemper, Alexandra Miller, Robert Pawlosky, M. Todd King, and Richard L. Veech. Mitigation of Damage from Reactive Oxygen Species and Ionizing Radiation by Ketone Body Esters. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0027.

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Reactive oxygen and nitrogen species, ROS and RNS, are ubiquitous in living cells. They have beneficial effects but are also the cause of a wide variety of diseases. However adding excessive amounts of reducing agents has a long history of clinical failure. This problem can be overcome by providing a novel ester of D-beta-hydroxybutyrate–R-1,3-butanediol, which is rapidly hydrolyzed to ketone bodies, the metabolism of which leads to the production of NADPH. The free cytosolic [NADP+]/[NADPH] redox potential is the most negative in the cell and sets the potential of the glutathione and ascorbic acid couples. Ketone bodies also act by inhibiting histone deacetylases, activating the transcription factor FOXO3 and increasing the transcription of enzymes involved in the destruction of ROS. Ketone esters would be effective in the treatment of a variety of disparate diseases where ROS play a role, ranging from Parkinson’s disease to radiation sickness and aging.

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14

Fink, Mitchell P. Ischaemia-reperfusion injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0308.

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Ischaemia/reperfusion (I/R) injury contributes to the pathogenesis of many common clinical conditions, including stroke, myocardial damage after percutaneous intervention for acute coronary artery occlusion, primary graft dysfunction after solid organ transplantation. The mechanisms that are responsible for I/R injury remain incompletely understood, but damage caused by reactive oxygen species (ROS) and reactive nitrogen species clearly is important. A number of therapeutic approaches, such as administration of ROS scavengers, are effective in animal models of I/R injury, but for the most part, translation of these findings into strategies that can clearly benefit patients has yet to be achieved.

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15

Vaziri, Nosratola D. Oxidative stress and its implications in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0112.

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Reactive oxygen species (ROS) are produced at low levels physiologically and their production conveys signals and has specific functions. Control mechanisms ensure that this does not cause damage. ROS are highly reactive and cytotoxic and are also deliberately produced by inflammatory cells (granulocytes, macrophages) to kill pathogens. If these chemicals are released inappropriately or excessively, or if control mechanisms are under-functioning, bystander or unintended tissue damage may be caused. The concept of oxidative stress is based on the idea that in certain states, commonly inflammatory states, release of oxygen radicals may be excessive, or control mechanisms weakened, so that tissue damage occurs. In CKD, both overproduction and diminished control may apply. No effective therapies acting via these pathways have been established so far though there remain some candidates.

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